Atorvastatin modulates the expression of aging-related genes in the brain of aging induced by D-galactose in mice | ||
| Iranian Journal of Basic Medical Sciences | ||
| دوره 24، شماره 10، دی 2021، صفحه 1388-1394 اصل مقاله (850.6 K) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2021.58502.12996 | ||
| نویسندگان | ||
| Manijeh Motevalian1، 2؛ Neda Tekyemaroof1؛ Mohammad Hadi Nematollahi3؛ Fatemeh Khajehasani4؛ Iman Fatemi* 5 | ||
| 1Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran | ||
| 2Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran | ||
| 3Department of Clinical Biochemistry, Kerman University of Medical Sciences, Kerman, Iran | ||
| 4Department of Radiology, Afzalipour Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran | ||
| 5Research Center of Tropical and Infectious Diseases, Kerman University of Medical Sciences, Kerman, Iran | ||
| چکیده | ||
| Objective(s): Atorvastatin (AT), a competitive inhibitor of 3-hydroxymethyl-3-glutaryl-coenzyme-A reductase, is a cholesterol-lowering drug. AT has been shown to have neuroprotective, antioxidant, and anti-inflammatory properties. Previously, we have reported that AT could attenuate the behavioral, renal, and hepatic manifestations of aging. To clarify further the mechanisms involved, the present study was designed to evaluate the effect of AT on the expression of some aging-related genes in the brain of aging mice induced by D-galactose (DG). Materials and Methods: For this purpose, AT (0.1 and 1 mg/kg/p.o.) was administrated daily in DG-received (500 mg/kg/p.o.) mice model of aging for six weeks. At the end of the experiment, mice were decapitated to remove the brains. Then, the expression profiles of sirtuin 1 (Sirt1), P53, P21, Bcl-2, Bax, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), interleukin 1 beta (IL1β), tumor necrosis factor-alpha (TNFα), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and brain-derived neurotrophic factor (BDNF) were assessed using the real-time PCR method. Results: The present study shows that DG decreases the expression of Sirt1, Bcl-2, CAT, GPx, and BDNF while increasing the expression of P53, P21, Bax, IL-1β, iNOS, COX-2, and TNF-α. According to the findings of the present study, AT (more potentially at the dose of 1 mg/kg) modulates the expression of these aging-related genes in the brain of aging mice. Conclusion: The results of the present study confirmed our previous reports on the anti-aging effects of AT at the gene level, the precise mechanisms and underlying pathways need further studies. | ||
| کلیدواژهها | ||
| Aging؛ Animal model؛ Apoptosis؛ Gene expression؛ Inflammation | ||
| مراجع | ||
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